Effects of Labetalol on Systemic and Pulmonary Haemodynamics at Rest and during Exercise in Hypertensive Patients

1978 ◽  
Vol 55 (s4) ◽  
pp. 279s-281s
Author(s):  
R. Fagard ◽  
A. Amery ◽  
T. Reybrouck ◽  
P. Lijnen ◽  
L. Billiet
Keyword(s):  
Heart Rate ◽  
Brachial Artery ◽  
Maximal Exercise ◽  
Peripheral Resistance ◽  
Plasma Renin ◽  
Exercise Heart Rate ◽  
Plasma Aldosterone Concentration ◽  
Hypertensive Patients ◽  
Artery Pressure ◽  
Pulmonary Haemodynamics

1. Labetalol was administered to 18 hypertensive patients for an average duration of 2·44 weeks, with an average final daily dose of 1·65 g. 2. Labetalol decreased resting heart rate by 16% and maximal exercise heart rate by 21%; the phenylephrine-induced rise of systolic brachial artery pressure was reduced by 36%. 3. During labetalol brachial artery pressure was lowered by 29/15 mmHg in the recumbent position, by 41/23 mmHg at rest sitting, and by 53/23 mmHg at maximal exercise; total peripheral resistance was not significantly affected at rest recumbent, but was reduced at sitting and at exercise; cardiac output decreased in all conditions. 4. Labetalol reduced mean pulmonary artery and capillary wedge pressures only in the sitting position. Pulmonary vascular resistance remained unchanged. 5. The drug produced significant decreases of plasma renin activity and of plasma aldosterone concentration.

Haemodynamic Profile of Angiotensin II Antagonism in Essential Hypertensive Patients

1979 ◽  
Vol 57 (s5) ◽  
pp. 119s-121s
Author(s):  
S. N. Hunyor ◽  
H. Larkin ◽  
Janet Rowe
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cardiac Output ◽  
Salt Intake ◽  
Peripheral Resistance ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Hypertensive Patients ◽  
Renin Angiotensin ◽  
Heart Rate Effect

1. The haemodynamic response to antagonistic (10 μg min−1 kg−1) and agonistic (40 μg min−1 kg−1) doses of saralasin was studied in young essential hypertensive patients. Blood pressure behaviour alone was thought to be inadequate to describe the response pattern. 2. Pre-saralasin setting of the renin-angiotensin axis was varied with salt intake (15 and 290 mmol of Na+/day) each for 10 days. This failed to influence blood pressure or plasma volume. 3. Antagonist blockade after low salt lowered blood pressure in three patients with the highest plasma renin values. Cardiac output rose in two of these, but it dropped in all others. 4. Decreases in cardiac output occurred with both doses of saralasin and even with suppression of the renin-angiotensin axis. This response is therefore unlikely to be due to removal of myocardial or venous angiotensin effects. 5. The renin-angiotensin system played a part in maintenance of blood pressure only with severe salt restriction and in a small proportion of cases. 6. No heart rate effect was seen with saralasin. 7. Blood pressure and total peripheral resistance responses were dependent on pre-(antagonist/ agonist) setting, but heart rate and cardiac output were not influenced by this factor.

Factors that alter the plasma renin activity of the marmot

1983 ◽  
Vol 244 (6) ◽  
pp. R823-R831
Author(s):  
W. J. Ray ◽  
M. L. Zatzman
Keyword(s):  
Heart Rate ◽  
Blood Flow ◽  
Mean Arterial Pressure ◽  
Plasma Renin Activity ◽  
Peripheral Resistance ◽  
Plasma Renin ◽  
Renin Activity ◽  
Low Doses ◽  
Control Data ◽  
Volume Load

The effects of low doses of norepinephrine (NE) and furosemide and a volume load (nonhibernators only) on plasma renin activity (PRA), mean arterial pressure (MAP), heart rate (HR), left renal (RBF) and right iliac (IBF) blood flow, cardiac index (CI), and total peripheral resistance (TPR) were determined in euthermic and hibernating marmots. In nonhibernating marmots NE produced an increase in CI and TPR and a decrease in RBF. In hibernators this dose of NE caused an increase in MAP, HR, and renal resistance, whereas it decreased PRA and did not alter iliac resistance. Furosemide infusions led to an increase in PRA in both groups and an increase in TPR in nonhibernators. The volume load in nonhibernators produced only a decrease in PRA. A comparison of control data from the two groups indicated that the renal and iliac beds contribute only a small portion to the increase in TPR that occurs during hibernation.

EXERCISE HEART RATE DURING TREADMILL TEST IS RELATED TO RENAL FUNCTIONAL RESERVE IN ESSENTIAL HYPERTENSIVE PATIENTS

2018 ◽  
Vol 36 (Supplement 1) ◽  
pp. e77-e78
Author(s):  
K. Damianaki ◽  
K. Tsioufis ◽  
K. Dimitriadis ◽  
D. Konstantinidis ◽  
T. Kalos ◽  
...  
Keyword(s):  
Heart Rate ◽  
Exercise Heart Rate ◽  
Treadmill Test ◽  
Functional Reserve ◽  
Hypertensive Patients ◽  
Renal Functional Reserve

Hemodynamic response to graded exercise after chronic beta-adrenergic blockade

1977 ◽  
Vol 42 (2) ◽  
pp. 133-138 ◽  
Author(s):  
T. Reybrouck ◽  
A. Amery ◽  
L. Billiet
Keyword(s):  
Cardiac Index ◽  
Maximal Exercise ◽  
Hemodynamic Response ◽  
Exercise Heart Rate ◽  
Adrenergic Blockade ◽  
Stroke Index ◽  
Working Capacity ◽  
Beta Adrenergic ◽  
Artery Pressure ◽  
Graded Exercise

The effect of sustained beta-adrenergic blockade (BB) on the hemodynamic response to graded exercise has been studied in 31 patients with high blood pressure. Hemodynamic investigations were conducted during a control period and were repeated after 1 mo of BB. Similar readjustments were observed at rest and during submaximal and maximal exercise. No significant change occurred in maximal physical working capacity during beta blockade. This resulted from hemodynamic readjustments. Maximal exercise heart rate was reduced by 34%, and this was compensated for by a 31% enhancement in stroke index. Consequently cardiac index decreased by only 14%. In the Fick equation the decrease in cardiac index was further compensated by an increase of the total arteriovenous O2 difference of 8%, thereby maintaining O2 delivery to the tissues. At maximal exercise mean brachial artery pressure dropped 14.5%, while mean pulmonary artery pressure increased by 20%. It is concluded that the compensatory action of the stroke volume, resulting from the interaction of an increased preload and a decreased impedance, played a major role in the hemodynamic readjustments following chronic BB to maintain maximal working capacity.

scholarly journals EXERCISE HEART RATE DURING TREADMILL TEST IS RELATED TO RENAL FUNCTIONAL RESERVE IN ESSENTIAL HYPERTENSIVE PATIENTS: A NOVEL LINK BETWEEN THE HEART AND THE KIDNEYS

2018 ◽  
Vol 71 (11) ◽  
pp. A1808
Author(s):  
Konstantinos P. Tsioufis ◽  
Kyriakos Dimitriadis ◽  
Katerina Damianaki ◽  
Dimitris Konstantinidis ◽  
Theodoros Kalos ◽  
...  
Keyword(s):  
Heart Rate ◽  
Exercise Heart Rate ◽  
Treadmill Test ◽  
Functional Reserve ◽  
Hypertensive Patients ◽  
Renal Functional Reserve

Development and Validation of Criteria for Sparing Confirmatory Tests in Diagnosing Primary Aldosteronism

2020 ◽  
Vol 105 (7) ◽  
pp. e2449-e2456 ◽  
Author(s):  
Kanran Wang ◽  
Jinbo Hu ◽  
Jun Yang ◽  
Ying Song ◽  
Peter J Fuller ◽  
...  
Keyword(s):  
Primary Aldosteronism ◽  
Challenge Test ◽  
Plasma Renin ◽  
Diagnostic Value ◽  
Endocrine Society ◽  
Plasma Aldosterone Concentration ◽  
Hypertensive Patients ◽  
Confirmatory Tests ◽  
Chinese Cohort ◽  
Development And Validation

Abstract Context The Endocrine Society Guidelines for the diagnosis of primary aldosteronism (PA) suggest that confirmatory tests (CFT) are not required when the following criteria are met: plasma aldosterone concentration (PAC) is >20 ng/dL, plasma renin is below detection levels, and hypokalemia is present. The evidence for the applicability of the guideline criteria is limited. Objective To develop and validate optimized criteria for sparing CFT in the diagnosis of PA. Design and Setting The optimized criteria were developed in a Chinese cohort using the captopril challenge test, verified by saline infusion test (SIT) and fludrocortisone suppression test (FST), and validated in an Australian cohort. Participants Hypertensive patients who completed PA screening and CFT. Main Outcome Measure Diagnostic value of the optimized criteria. Results In the development cohort (518 PA and 266 non-PA), hypokalemia, PAC, and plasma renin concentration (PRC) were selected as diagnostic indicators by multivariate logistic analyses. The combination of PAC >20 ng/dL plus PRC <2.5 μIU/mL plus hypokalemia had much higher sensitivity than the guideline criteria (0.36 vs 0.11). The optimized criteria remained superior when the SIT or FST were used as CFT. Non-PA patients were not misdiagnosed by either criteria, but the percentage of patients in whom CFT could be spared was higher with the optimized criteria. In the validation cohort (125 PA and 81 non-PA), the sensitivity of the optimized criteria was also significantly higher (0.12 vs 0.02). Conclusions Hypertensive patients with PAC >20 ng/dL, PRC <2.5 μIU/mL, plus hypokalemia can be confidently diagnosed with PA without confirmatory tests.

Hemodynamic effects of neurohypophyseal peptides with antidiuretic activity in dogs

1985 ◽  
Vol 249 (5) ◽  
pp. H1001-H1008 ◽  
Author(s):  
J. Schwartz ◽  
J. F. Liard ◽  
C. Ott ◽  
A. W. Cowley
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Plasma Renin Activity ◽  
Peripheral Resistance ◽  
Cardiovascular Effects ◽  
Plasma Renin ◽  
Hemodynamic Effects ◽  
Antidiuretic Activity

Arginine vasopressin (AVP) is known to produce increases in total peripheral resistance (TPR) and mean arterial pressure (MAP) and decreases in heart rate (HR), cardiac output (CO), and plasma renin activity (PRA). Some recent observations with AVP and synthetic analogues have suggested that under certain conditions, AVP can induce cardiovascular and reninsecretory responses in the opposite directions. To characterize the receptors mediating these responses, the effects of AVP, oxytocin, and synthetic neurohypophyseal analogues with specific antidiuretic, vasoconstrictor, or oxytocic activities were studied in conscious dogs. AVP and 2-phenylalanine-8-ornithine-oxytocin (Phe2Orn8OT, a selective vasoconstrictor agonist) produced similar responses when infused at 10 ng X kg-1 X min-1. That is, TPR and MAP increased, and CO, HR, and PRA decreased. Pretreatment with a selective vasoconstrictor antagonist, [1-(beta-mercapto-beta,beta-cyclopentamethylenepropionic acid) 2-(O-methyl)tyrosine]AVP, abbreviated d(CH2)5Tyr(Me)-AVP (10 micrograms/kg), blocked the actions of Phe2Orn8OT. However, in the presence of d(CH2)5Tyr(Me)AVP, AVP actually decreased TPR and increased CO, HR, and PRA. An analogue with selective antidiuretic activity, 4-valine-8-D-AVP (VDAVP, 10 ng X kg-1 X min-1), produced the same effects as the combination of vasopressin plus d(CH2)5Tyr(Me)AVP. Neither the effects of VDAVP nor of AVP plus antagonist were blocked by propranolol (1 mg/kg). These data indicate that vasopressin, by its antidiuretic activity, produces cardiovascular effects that are opposite to many of those produced by its vasoconstrictor action and that these effects are not dependent on mediation by beta-adrenoceptors.

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